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Transcriptomic analysis for understanding differential gene expression upon FKBP5 knockdown

ABSTRACT: Transcriptomic analysis for understanding differential gene expression upon FKBP5 knockdown

PROVIDER: PRJNA716642 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14049007_1.fastq.gz	Fastqsanger.gz
	SRR14049007_2.fastq.gz	Fastqsanger.gz
	SRR14049008_1.fastq.gz	Fastqsanger.gz
	SRR14049008_2.fastq.gz	Fastqsanger.gz

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Transcriptomic analysis for understanding differential gene expression upon FKBP5 knockdown

Project description:To investigate differentially expressed genes in HEK293T cells upon FKBP5 knockdown (n =2, reported in this study) and control scramble (n=2) (reported earlier Yadav et al., Cell Reports 2019, NCBI Genbank SRA accession no. PRJNA512165) using total RNA extracted from HEK293T cells and analysed by RNA-seq.

2021-03-24 | GSE169461 | GEO

Stress responsive gene FKBP5 mediates alcohol-induced liver injury through hippo pathway and CXCL1 signaling

Project description:To better our understanding and obtain a mechanistic insight on the role of FKBP5 on alcohol-induced liver injury, we performed RNA-seq analysis and compared the alterations in gene expression from WT and Fkbp5-/- mice on ethanol and pair-fed diet.

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Corticosteroid-induced chromatin loop dynamics at the FKBP5 gene

Project description:FKBP5 is a long glucocorticoid-inducible gene implicated in psychiatric disorders. To investigate the complexities of chromatin interaction frequencies at the FKBP5 topologically associated domain (TAD), we deployed fifteen one-to-all chromatin capture viewpoints near gene promoters, enhancers, introns, and CTCF-loop anchors. This revealed a ‘one-TAD-one-gene’ structure encompassing the FKBP5 promoter and its enhancers. The FKBP5 promoter and its two glucocorticoid-stimulated enhancers roam the entire TAD while displaying subtle cell type-specific interactomes. The FKBP5 TAD consists of two nested CTCF loops that are coordinated by one CTCF site beyond the FKBP5 polyadenylation site and another in its 8th intron, 61 kb further. Loop extension correlates with transcription increases through the intronic CTCF site. This is efficiently compensated for, since the short loop is restored even under high transcription regimes. The boundaries of the FKBP5 TAD consist of divergent CTCF sites, harbor multiple smaller genes and are resilient to glucocorticoid stimulation. Interestingly, both FKBP5 TAD boundaries harbor H3K27me3-marked heterochromatin blocks that may reinforce them. We propose that cis-acting genetic and epigenetic polymorphisms underlying FKBP5 expression variation are likely to reside within a 240 kb region that consists of the FKBP5 TAD, its left sub-TAD, and both its boundaries.

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micro RNA expression analysis in the prefrontal cortex of Fkbp5 deficient mice

Project description:Psychological stress is a risk factor for several diseases. In particular, stressor exposure has been linked with various psychiatric disorders. Since the hypothalamic-pituitary-adrenal (HPA) axis plays a central role in the regulation of stress responses, it has been implicated in the etiology of stress related disorders such as PTSD. The HPA axis regulate synthesis and release of glucocorticoids and its dysregulation cause abnormal response to stress. FK506-binding protein 51 (FKBP5) is a co chaperone of HSP90 in the glucocorticoid receptor (GR) molecular complex and a key regulator of the sensitivity of GR. In this study, we profiled the miRNAs in the prefrontal cortex of FKBP5 knock out mice compared to the wild type. Subsequently, we profiled target mRNAs for differentially expressed miRNAs in the FKBP5 deficient mice using several tools for sequence-based miRNA target prediction such as miRDB, DIANA tool, miRmap and TargetScan. Gene ontology analysis suggested that differentially expressed miRNAs in the brain of FKBP5 deficient mice may be involved in neuron development, cell motion, endocytosis, and cell-cell adhesion. These results suggest that Nfasc could be a new target for understanding of the pathophysiology of PTSD.

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